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26 Cards in this Set

  • Front
  • Back
Metabolic syndrome/syndrome X
t2dm
+
dyslipidemia
+
cardiovascular disease
+
hypertension
Type 1 diabetes

(insulin dependent)
autoimmune destruction of pancreatic b cells
In UK ____ of population have diabetes
3.7%
Diabetes is the major cause of ....
Kidney Failure
Cardiovascular Disease
Non-traumatic Amputation
Blindness
Type 2 diabetes

(non-insulin dependent)
>90% of cases
10% of US have it
4th cause of death in the world
oral hypoglycaemics
enhance b cell function
lipolysis
breakdown of lipids to produce free fatty acids
insulin resistance
->
_____________
->
_____________
=
DIABETES
hyperinsulinemia (b cell compensation)

hyperglycaemia (b cell degeneration - cannot cope with glc demand)
For glucose homeostasis....

glc levels are senses by ______, ___ and b cells

glc is disposed via _____, ______ and liver
brain
gut
muscle
adipose
parasympathetic nerves ->
improved b cell function
sympathetic nerves ->
decreased b cell function (i.e insulin)
incretins from gut
improve b cell function
metabolic actions of insulin

1) Glc uptake

2) _______ _______

3) Promote Glycolysis

4) ___ & ___ _______
glycogen synthesis
- activates glycogen synthase
-inhibits glycogen phosphorylase

3)
- activates glucokinase, PFK, PK, PDH

3) FA & TG synthesis
-activate ATP-citrate lyase
-activates Ac-CoA carboxylase
-inhibits HSL
b cell releases insulin in response to ______ ______ ____
increased glucose levels
high [glc]
->
high [Acetyl-coA]
->
high [Malonyl-coA]
->
__________
inhibits FA oxidation

promotes glc oxidation
AMPK inhibits
acetyl-coA carboxylase
malonyl-coA inhibits
transport of FA into mitochondia (for oxidation)
randle cycle
"glucose-fatty acid cycle" to describe fuel flux between and fuel selection by tissues
glucose disposal in muscle
GLYCOLYSIS-> crebs cycle -> ATP
glycogen synthesis
glucose disposal in adipose
glycolysis---> FA & TG synthesis
glucose disposal in liver
GLYCOGEN SYNTHESIS
FA & TG synthesis
insulin in liver
inhibits GLUCONEOGENESIS
increases glucose uptake
increases glycogen and FA synthesis
insulin in adipose
enhances differentiation
inhibits lipolysis (via HSL)
increases lipogenesis
increase glc uptake
insulin in skeletal muscle
increase glc uptake
promote glycolysis
promote glycogen synthesis
KO of IR component in b cells ->
T2DM
Insulin resistance ->
decreased glucose uptake and disposal
- inhibition of GLUT 4 and glucokinase

Gluconeogenesis
- via activation of PEPCK

Hyperlipidemia
- increase circulating FFA, VLDL via inhibition of adipocyte differentiation/ activation of HSL

HYPERGLYCAEMIA via b cell dysfunction!!!